Dietary salt influences postprandial plasma sodium concentration and systolic blood pressure

Suckling, Rebecca; He, Feng J; Markandu, Nirmala D.; MacGregor, Graham A.

doi:10.1038/ki.2011.369

Cited by 118 publications

(86 citation statements)

References 23 publications

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“…Higher SNa could be a readout for higher sodium intake. This hypothesis would agree with an acute increase in the SNa concentration observed under salt load in normotensive, healthy volunteers [121], however recent evidence suggests higher dietary salt intake may not be associated with higher SNa in HD patients [122]. Figure 3b demonstrates a negative association between predialysis SNa and IDWG, shown also in our analyses from the DOPPS [79,81].…”

Section: Association Between Predialysis Serum Sodium and Volume Oversupporting

confidence: 76%

Significance of Interdialytic Weight Gain versus Chronic Volume Overload: Consensus Opinion

et al. 2013

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Predialysis volume overload is the sum of interdialytic weight gain (IDWG) and residual postdialysis volume overload. It results mostly from failure to achieve an adequate volume status at the end of the dialysis session. Recent developments in bioimpedance spectroscopy and possibly relative plasma volume monitoring permit noninvasive volume status assessment in hemodialysis patients. A large proportion of patients have previously been shown to be chronically volume overloaded predialysis (defined as >15% above ‘normal' extracellular fluid volume, equivalent to >2.5 liters on average), and to exhibit a more than twofold increased mortality risk. By contrast, the magnitude of the mortality risk associated with IDWG is much smaller and only evident with very large weight gains. Here we review the available evidence on volume overload and IDWG, and question the use of IDWG as an indicator of ‘nonadherence' by describing its association with postdialysis volume depletion. We also demonstrate the relationship between IDWG, volume overload and predialysis serum sodium concentration, and comment on salt intake. Discriminating between volume overload and IDWG will likely lead to a more appropriate management of fluid withdrawal during dialysis. Consensually, the present authors agree that this discrimination should be among the primary goals for dialysis caretakers today. In consequence, we recommend objective measures of volume status beyond mere evaluations of IDWG.

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Section: Association Between Predialysis Serum Sodium and Volume Oversupporting

confidence: 76%

Significance of Interdialytic Weight Gain versus Chronic Volume Overload: Consensus Opinion

et al. 2013

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“…EnNaC endothelial Na + channel concluded that high salt intake compromises the responsiveness of endothelial cells to shear stress [9,10,70]. Studies in humans confirmed what has been learned from animal models: a high-Na + diet (300-350 mmol/day) led to an increase in plasma [Na + ] of 2-4 mmol/l and thus to a loss of NOdependent vasodilation [32,123].…”

Section: Salt Intake Affects Endothelial Functionmentioning

confidence: 51%

Salt controls endothelial and vascular phenotype

Kusche-Vihrog

Schmitz

Brand

2014

Pflugers Arch - Eur J Physiol

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High salt (NaCl) intake promotes the development of vascular diseases independent of a rise in blood pressure, whereas reduction of salt consumption has beneficial effects for the arterial system. This article summarizes our current understanding of the molecular mechanisms of high salt-induced alterations of the endothelial phenotype, the impact of the individual endothelial genotype, and the overall vascular phenotype. We focus on the endothelial Na(+) channel (EnNaC)-controlled nanomechanical properties of the endothelium, since high Na(+) leads to an EnNaC-induced Na(+)-influx and subsequent stiffening of endothelial cells. The mechanical stiffness of the endothelial cell (i.e., the endothelial phenotype) plays a crucial role as it controls the production of the endothelium-derived vasodilator nitric oxide (NO) which directly affects the tone of the vascular smooth muscle cells. In contrast to soft endothelial cells, stiff endothelial cells release reduced amounts of NO, the hallmark of endothelial dysfunction. This endothelium-born process is followed by the development of arterial stiffness (i.e., the vascular phenotype), predicting the development of vascular end-organ damage such as myocardial infarction, stroke, and renal impairment. In this context, we outline the potential clinical implication of direct (amiloride) and indirect (spironolactone) EnNaC inhibition on vascular function. However, interindividual differences exist in the response to high salt intake which involves different endothelial genotypes. Thus, selected genes and genetic variants contributing to the development of salt-induced endothelial dysfunction and hypertension are discussed. In this review, we focus on the role of salt in endothelial and vascular (dys)function and the link between salt-induced changes of the endothelial and vascular phenotype and its clinical implications.

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“…49 This hypothesis is supported by a number of animal studies; in fact, neonatal uni nephrectomy causes hypertension in adult rats. 17,18 In one human autopsy study in which nephron number was counted, 10 white middle-aged individuals with hypertension had fewer nephrons than did 10 well-matched controls without hypertension. 51 Other autopsy studies that included both Caucasians and African Americans confirmed the association between reduced glomerular number and hypertension in Caucasians but not in African Americans.…”

Section: Nephron Mass and Hypertensionmentioning

confidence: 99%

“…For most individuals, an increase in salt intake induces only a modest and transient rise in arterial pressure. 18 However, the ability of the kidney to adapt to variable intake of sodium differs between indivi duals and is influenced by both genetic and environmental factors. Some individuals are designated as salt sensitive and respond to a high-salt diet with a large rise in blood pressure indicative of a blunted pressure-natriuresis relation ship.…”

Section: Impaired Tubular Handling Of Sodiummentioning

confidence: 99%

The role of the kidney in regulating arterial blood pressure

2012

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The kidney plays a central role in the regulation of arterial blood pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal perfusion pressure are closely involved in maintaining the arterial circulation and blood pressure. Renal artery perfusion pressure directly regulates sodium excretion-a process known as pressure natriuresis-and influences the activity of various vasoactive systems such as the renin-angiotensin-aldosterone system. As a result, many researchers argue that identifying any marked rise in blood pressure requires resetting of the relationship between arterial blood pressure and urinary sodium excretion, which can occur by an array of systemic or local mechanisms. Almost all of the monogenic forms of hypertension affect sites in the kidney associated with sodium handling and transport. Experimental models of spontaneous hypertension, such as the Dahl salt-sensitive rat, have been used to study the effects of kidney transplantation on blood pressure. Results from studies of kidney transplantation indicate that pressure sensitivity to sodium intake 'follows' the kidney, meaning that the recipient of a 'salt-resistant kidney' acquires sodium resistance, and that the recipient of a 'salt-sensitive kidney' acquires pressure sensitivity. The examples above and discussed in this Review demonstrate that it should come as no surprise that most disorders that affect the kidney or the renal vasculature commonly lead to secondary forms of hypertension.

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Dietary salt influences postprandial plasma sodium concentration and systolic blood pressure

Cited by 118 publications

References 23 publications

Significance of Interdialytic Weight Gain versus Chronic Volume Overload: Consensus Opinion

Significance of Interdialytic Weight Gain versus Chronic Volume Overload: Consensus Opinion

Salt controls endothelial and vascular phenotype

The role of the kidney in regulating arterial blood pressure

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